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The inflammatory markers in AKI patients treated by RRT and in controls.
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SE-associated LINC01013 was transcriptionally activated by <t>CEBPB</t> in hPASMCs. A Prediction of candidate transcription factors and binding sites. (Transcription factor related databases: JASPAR: https://jaspar.elixir.no/ ; PROMO: https://alggen.lsi.upc.es/cgi-bin/promo_v3/promo/promoinit.cgi?dirDB=TF_8.3 ; GENECARD: https://www.genecards.org/ ; AnimalTFDB: http://bioinfo.life.hust.edu.cn/HumanTFDB/#!/ ; Super enhancer related database: LncSEA: https://bio.liclab.net/LncSEA/ ). B The schematic diagram illustrates the LINC01013 promoter, divided into segments P1-P4, and the binding sites of transcription factors. C Four constituents (E1-E4) of SE region of LINC01013 derived from the WashU Epigenome Browser databases ( http://epigenomegateway.wustl.edu/browser/ ). D , E hPASMCs were subjected to ChIP analysis using antibodies <t>against</t> <t>H3K27ac,</t> H3K4me1 and CEBPB. The association with the SE region (D, E1-E4) and promoter region (E, P1-P4) of LINC01013 was quantified by RT‒qPCR ( n = 3). F hPASMCs were treated with CEBPB siRNA and subjected to ChIP analysis using antibodies against H3K27ac. The association with the E2 of SE (left) and P1-P3 promoter regions (right) of LINC01013 was quantified by RT-qPCR ( n = 3). G Schematic diagram of transcribing LINC01013 in hPASMCs. All values are presented as the mean ± SEM. Statistical analysis was performed with one-way ANOVA or Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001. Nor, normoxia; Hyp, hypoxia; NC, negative control; IP, immunoprecipitation; IgG, Immunoglobulin G; TSS, transcription initiation site
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SE-associated LINC01013 was transcriptionally activated by <t>CEBPB</t> in hPASMCs. A Prediction of candidate transcription factors and binding sites. (Transcription factor related databases: JASPAR: https://jaspar.elixir.no/ ; PROMO: https://alggen.lsi.upc.es/cgi-bin/promo_v3/promo/promoinit.cgi?dirDB=TF_8.3 ; GENECARD: https://www.genecards.org/ ; AnimalTFDB: http://bioinfo.life.hust.edu.cn/HumanTFDB/#!/ ; Super enhancer related database: LncSEA: https://bio.liclab.net/LncSEA/ ). B The schematic diagram illustrates the LINC01013 promoter, divided into segments P1-P4, and the binding sites of transcription factors. C Four constituents (E1-E4) of SE region of LINC01013 derived from the WashU Epigenome Browser databases ( http://epigenomegateway.wustl.edu/browser/ ). D , E hPASMCs were subjected to ChIP analysis using antibodies <t>against</t> <t>H3K27ac,</t> H3K4me1 and CEBPB. The association with the SE region (D, E1-E4) and promoter region (E, P1-P4) of LINC01013 was quantified by RT‒qPCR ( n = 3). F hPASMCs were treated with CEBPB siRNA and subjected to ChIP analysis using antibodies against H3K27ac. The association with the E2 of SE (left) and P1-P3 promoter regions (right) of LINC01013 was quantified by RT-qPCR ( n = 3). G Schematic diagram of transcribing LINC01013 in hPASMCs. All values are presented as the mean ± SEM. Statistical analysis was performed with one-way ANOVA or Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001. Nor, normoxia; Hyp, hypoxia; NC, negative control; IP, immunoprecipitation; IgG, Immunoglobulin G; TSS, transcription initiation site
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SE-associated LINC01013 was transcriptionally activated by <t>CEBPB</t> in hPASMCs. A Prediction of candidate transcription factors and binding sites. (Transcription factor related databases: JASPAR: https://jaspar.elixir.no/ ; PROMO: https://alggen.lsi.upc.es/cgi-bin/promo_v3/promo/promoinit.cgi?dirDB=TF_8.3 ; GENECARD: https://www.genecards.org/ ; AnimalTFDB: http://bioinfo.life.hust.edu.cn/HumanTFDB/#!/ ; Super enhancer related database: LncSEA: https://bio.liclab.net/LncSEA/ ). B The schematic diagram illustrates the LINC01013 promoter, divided into segments P1-P4, and the binding sites of transcription factors. C Four constituents (E1-E4) of SE region of LINC01013 derived from the WashU Epigenome Browser databases ( http://epigenomegateway.wustl.edu/browser/ ). D , E hPASMCs were subjected to ChIP analysis using antibodies <t>against</t> <t>H3K27ac,</t> H3K4me1 and CEBPB. The association with the SE region (D, E1-E4) and promoter region (E, P1-P4) of LINC01013 was quantified by RT‒qPCR ( n = 3). F hPASMCs were treated with CEBPB siRNA and subjected to ChIP analysis using antibodies against H3K27ac. The association with the E2 of SE (left) and P1-P3 promoter regions (right) of LINC01013 was quantified by RT-qPCR ( n = 3). G Schematic diagram of transcribing LINC01013 in hPASMCs. All values are presented as the mean ± SEM. Statistical analysis was performed with one-way ANOVA or Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001. Nor, normoxia; Hyp, hypoxia; NC, negative control; IP, immunoprecipitation; IgG, Immunoglobulin G; TSS, transcription initiation site
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SE-associated LINC01013 was transcriptionally activated by <t>CEBPB</t> in hPASMCs. A Prediction of candidate transcription factors and binding sites. (Transcription factor related databases: JASPAR: https://jaspar.elixir.no/ ; PROMO: https://alggen.lsi.upc.es/cgi-bin/promo_v3/promo/promoinit.cgi?dirDB=TF_8.3 ; GENECARD: https://www.genecards.org/ ; AnimalTFDB: http://bioinfo.life.hust.edu.cn/HumanTFDB/#!/ ; Super enhancer related database: LncSEA: https://bio.liclab.net/LncSEA/ ). B The schematic diagram illustrates the LINC01013 promoter, divided into segments P1-P4, and the binding sites of transcription factors. C Four constituents (E1-E4) of SE region of LINC01013 derived from the WashU Epigenome Browser databases ( http://epigenomegateway.wustl.edu/browser/ ). D , E hPASMCs were subjected to ChIP analysis using antibodies <t>against</t> <t>H3K27ac,</t> H3K4me1 and CEBPB. The association with the SE region (D, E1-E4) and promoter region (E, P1-P4) of LINC01013 was quantified by RT‒qPCR ( n = 3). F hPASMCs were treated with CEBPB siRNA and subjected to ChIP analysis using antibodies against H3K27ac. The association with the E2 of SE (left) and P1-P3 promoter regions (right) of LINC01013 was quantified by RT-qPCR ( n = 3). G Schematic diagram of transcribing LINC01013 in hPASMCs. All values are presented as the mean ± SEM. Statistical analysis was performed with one-way ANOVA or Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001. Nor, normoxia; Hyp, hypoxia; NC, negative control; IP, immunoprecipitation; IgG, Immunoglobulin G; TSS, transcription initiation site
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Macrophage activation caused inflammation of lung tissue in response to PM 2 . 5 . (A) Immunohistochemistry detection of the macrophage marker F4/80 in mouse lung tissues. Scale bar = 10 μm. (B) Pathological changes in the lung tissues. Scale bar = 10 μm. (C , D) Western blot analysis of TNF-α and IL-1β levels in the lung tissues. The plot gives a quantitative gray-scale analysis of the blot ( n = 3). (E) <t>ELISA</t> analysis of IL-6 in serum ( n = 5). (F) Real-time quantitative PCR analysis of IL-6, TNF-α, and IL-1β in the lung ( n = 8). (G , H) Western blot analysis of the P-PI3K, P-AKT, and NF-κB in mouse lung tissues. The plot gives a quantitative gray-scale analysis of the blot ( n = 3). (I) Immunohistochemistry detection of P-AKT and NF-κB in mouse lung tissues. Scale bar = 10 μm. Data are the means ± SEMs from at least three independent experiments, each performed in triplicate. * P < 0.5 and ** P < 0.01—levels of significance that are different from the control group at the levels, respectively.
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Macrophage activation caused inflammation of lung tissue in response to PM 2 . 5 . (A) Immunohistochemistry detection of the macrophage marker F4/80 in mouse lung tissues. Scale bar = 10 μm. (B) Pathological changes in the lung tissues. Scale bar = 10 μm. (C , D) Western blot analysis of TNF-α and IL-1β levels in the lung tissues. The plot gives a quantitative gray-scale analysis of the blot ( n = 3). (E) <t>ELISA</t> analysis of IL-6 in serum ( n = 5). (F) Real-time quantitative PCR analysis of IL-6, TNF-α, and IL-1β in the lung ( n = 8). (G , H) Western blot analysis of the P-PI3K, P-AKT, and NF-κB in mouse lung tissues. The plot gives a quantitative gray-scale analysis of the blot ( n = 3). (I) Immunohistochemistry detection of P-AKT and NF-κB in mouse lung tissues. Scale bar = 10 μm. Data are the means ± SEMs from at least three independent experiments, each performed in triplicate. * P < 0.5 and ** P < 0.01—levels of significance that are different from the control group at the levels, respectively.
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UHMWPE increased the expression of <t>mIL-6R</t> protein. FLS cells were incubated with UHMWPE (0, 0.01, 0.1, and 1g/L) for 7 d. The expression of <t>IL-6R</t> protein was detected by western blotting assay.
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Image Search Results


The inflammatory markers in AKI patients treated by RRT and in controls.

Journal: BMC Nephrology

Article Title: Malnutrition and inflammation in acute kidney injury due to earthquake-related crush syndrome

doi: 10.1186/1471-2369-11-4

Figure Lengend Snippet: The inflammatory markers in AKI patients treated by RRT and in controls.

Article Snippet: The serum C-reactive protein (CRP), prealbumin, and transferrin levels were measured in participants in Group C and Group E. Interleukin 6 (IL-6) (Wuhan Boster Biological Technology, China) and tumor necrosis factor-α (TNF-α) (Wuhan Boster Biological Technology, China) levels were tested by enzyme-linked immunosorbent assay (ELISA) methods in accordance with the specifications of the manufacturers in Group E and in 18 participants from Group C who received RRT and were followed for more than 14 days.

Techniques:

SE-associated LINC01013 was transcriptionally activated by CEBPB in hPASMCs. A Prediction of candidate transcription factors and binding sites. (Transcription factor related databases: JASPAR: https://jaspar.elixir.no/ ; PROMO: https://alggen.lsi.upc.es/cgi-bin/promo_v3/promo/promoinit.cgi?dirDB=TF_8.3 ; GENECARD: https://www.genecards.org/ ; AnimalTFDB: http://bioinfo.life.hust.edu.cn/HumanTFDB/#!/ ; Super enhancer related database: LncSEA: https://bio.liclab.net/LncSEA/ ). B The schematic diagram illustrates the LINC01013 promoter, divided into segments P1-P4, and the binding sites of transcription factors. C Four constituents (E1-E4) of SE region of LINC01013 derived from the WashU Epigenome Browser databases ( http://epigenomegateway.wustl.edu/browser/ ). D , E hPASMCs were subjected to ChIP analysis using antibodies against H3K27ac, H3K4me1 and CEBPB. The association with the SE region (D, E1-E4) and promoter region (E, P1-P4) of LINC01013 was quantified by RT‒qPCR ( n = 3). F hPASMCs were treated with CEBPB siRNA and subjected to ChIP analysis using antibodies against H3K27ac. The association with the E2 of SE (left) and P1-P3 promoter regions (right) of LINC01013 was quantified by RT-qPCR ( n = 3). G Schematic diagram of transcribing LINC01013 in hPASMCs. All values are presented as the mean ± SEM. Statistical analysis was performed with one-way ANOVA or Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001. Nor, normoxia; Hyp, hypoxia; NC, negative control; IP, immunoprecipitation; IgG, Immunoglobulin G; TSS, transcription initiation site

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Super enhancer-driven LINC01013 mediates hypoxia-induced mitochondrial dysfunction by HSPA9 to determine pulmonary arterial smooth muscle cell fate

doi: 10.1007/s00018-025-06071-3

Figure Lengend Snippet: SE-associated LINC01013 was transcriptionally activated by CEBPB in hPASMCs. A Prediction of candidate transcription factors and binding sites. (Transcription factor related databases: JASPAR: https://jaspar.elixir.no/ ; PROMO: https://alggen.lsi.upc.es/cgi-bin/promo_v3/promo/promoinit.cgi?dirDB=TF_8.3 ; GENECARD: https://www.genecards.org/ ; AnimalTFDB: http://bioinfo.life.hust.edu.cn/HumanTFDB/#!/ ; Super enhancer related database: LncSEA: https://bio.liclab.net/LncSEA/ ). B The schematic diagram illustrates the LINC01013 promoter, divided into segments P1-P4, and the binding sites of transcription factors. C Four constituents (E1-E4) of SE region of LINC01013 derived from the WashU Epigenome Browser databases ( http://epigenomegateway.wustl.edu/browser/ ). D , E hPASMCs were subjected to ChIP analysis using antibodies against H3K27ac, H3K4me1 and CEBPB. The association with the SE region (D, E1-E4) and promoter region (E, P1-P4) of LINC01013 was quantified by RT‒qPCR ( n = 3). F hPASMCs were treated with CEBPB siRNA and subjected to ChIP analysis using antibodies against H3K27ac. The association with the E2 of SE (left) and P1-P3 promoter regions (right) of LINC01013 was quantified by RT-qPCR ( n = 3). G Schematic diagram of transcribing LINC01013 in hPASMCs. All values are presented as the mean ± SEM. Statistical analysis was performed with one-way ANOVA or Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001. Nor, normoxia; Hyp, hypoxia; NC, negative control; IP, immunoprecipitation; IgG, Immunoglobulin G; TSS, transcription initiation site

Article Snippet: The antibody against CEBPB (PB9171, BA0670, 1:500, Boster, Wuhan, China), H3K27ac (A7253, 1:500, ABclonal, Wuhan, China), H3K4me1 (A2355, 1:500, Wuhan, China), PCNA (A00125, 1:500, Boster, Wuhan, China), Cyclin A (PB0515, 1:500, Boster, Wuhan, China), Cyclin D (BM4272, 1:500, Boster, Wuhan, China), IL-6 (AF7236, 1:500, Beyotime, Shanghai, China), TNF-α (AF8208, 1:500, Beyotime, Shanghai, China), PKM2 (4053, 1:1000, Cell Signaling, MA, US), HK II (66974-1-Ig, 1:1000, Proteintech, IL, USA), PDH (2784, 1:1000, Cell Signaling, MA, US), HSPA9 (14887-1-AP, 1:5000, Proteintech, IL, USA), VDAC1 (10866-1-AP, 1:5000, Proteintech, IL, USA), and β-actin (TA-09, 1:1000, ZSGB‐BIO, Beijing, China) was incubated at 4 °C overnight, followed by incubation with appropriate horseradish peroxidase-conjugated secondary antibodies at room temperature for 1 h, and proteins were visualized with enhanced chemiluminescence reagents.

Techniques: Binding Assay, Derivative Assay, Quantitative RT-PCR, Negative Control, Immunoprecipitation

Macrophage activation caused inflammation of lung tissue in response to PM 2 . 5 . (A) Immunohistochemistry detection of the macrophage marker F4/80 in mouse lung tissues. Scale bar = 10 μm. (B) Pathological changes in the lung tissues. Scale bar = 10 μm. (C , D) Western blot analysis of TNF-α and IL-1β levels in the lung tissues. The plot gives a quantitative gray-scale analysis of the blot ( n = 3). (E) ELISA analysis of IL-6 in serum ( n = 5). (F) Real-time quantitative PCR analysis of IL-6, TNF-α, and IL-1β in the lung ( n = 8). (G , H) Western blot analysis of the P-PI3K, P-AKT, and NF-κB in mouse lung tissues. The plot gives a quantitative gray-scale analysis of the blot ( n = 3). (I) Immunohistochemistry detection of P-AKT and NF-κB in mouse lung tissues. Scale bar = 10 μm. Data are the means ± SEMs from at least three independent experiments, each performed in triplicate. * P < 0.5 and ** P < 0.01—levels of significance that are different from the control group at the levels, respectively.

Journal: Frontiers in Cell and Developmental Biology

Article Title: lncRNA Gm16410 Mediates PM 2 . 5 -Induced Macrophage Activation via PI3K/AKT Pathway

doi: 10.3389/fcell.2021.618045

Figure Lengend Snippet: Macrophage activation caused inflammation of lung tissue in response to PM 2 . 5 . (A) Immunohistochemistry detection of the macrophage marker F4/80 in mouse lung tissues. Scale bar = 10 μm. (B) Pathological changes in the lung tissues. Scale bar = 10 μm. (C , D) Western blot analysis of TNF-α and IL-1β levels in the lung tissues. The plot gives a quantitative gray-scale analysis of the blot ( n = 3). (E) ELISA analysis of IL-6 in serum ( n = 5). (F) Real-time quantitative PCR analysis of IL-6, TNF-α, and IL-1β in the lung ( n = 8). (G , H) Western blot analysis of the P-PI3K, P-AKT, and NF-κB in mouse lung tissues. The plot gives a quantitative gray-scale analysis of the blot ( n = 3). (I) Immunohistochemistry detection of P-AKT and NF-κB in mouse lung tissues. Scale bar = 10 μm. Data are the means ± SEMs from at least three independent experiments, each performed in triplicate. * P < 0.5 and ** P < 0.01—levels of significance that are different from the control group at the levels, respectively.

Article Snippet: Mouse IL-6 ELISA kit was purchased from Boster (Wuhan, China).

Techniques: Activation Assay, Immunohistochemistry, Marker, Western Blot, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction, Control

UHMWPE increased the expression of mIL-6R protein. FLS cells were incubated with UHMWPE (0, 0.01, 0.1, and 1g/L) for 7 d. The expression of IL-6R protein was detected by western blotting assay.

Journal: BioMed Research International

Article Title: The Role of IL-6RA in UHMWPE Promotes Proliferation in Fibro-Like Synovial Cells

doi: 10.1155/2018/3928915

Figure Lengend Snippet: UHMWPE increased the expression of mIL-6R protein. FLS cells were incubated with UHMWPE (0, 0.01, 0.1, and 1g/L) for 7 d. The expression of IL-6R protein was detected by western blotting assay.

Article Snippet: The primary antibodies included caspase-3(Abcam, USA; ab4051), cleaved-caspase-3 (Cell Signaling Technology, USA; #9661), Bax (Abcam, USA; ab182733), Bcl-2 (Abcam, USA; ab692), IL-6R (Boster, China; A01425-1), β -actin (Bioss, China; bs-0061R), and GAPDH (Abcam, USA; ab8245) at 1:500 dilutions.

Techniques: Expressing, Incubation, Western Blot